Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Signaling in microglia during CAR Tcell induced Immune cell associated neurotoxicity syndrome (ICANS)

ABSTRACT: Signaling in microglia during CAR Tcell induced Immune cell associated neurotoxicity syndrome (ICANS)

PROVIDER: PRJNA937671 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Microglia activation during CAR T cell induced neurotoxicity is dependent on TGF-β-activated kinase-1

Project description:Treatment with chimeric antigen receptor (CAR) T-cell therapy targeting CD19 (CAR19) can cause neurotoxicity in patients. The role of microglia in CAR19-induced neurotoxicity was unclear. We observed morphological microglia alterations, increased production of GM-CSF, MCP-1 and TNF by microglia and neurocognitive deficits in B-cell lymphoma-bearing mice upon CAR19 transfer. Gene expression analysis was performed to determine the microglial activation and downstream signalling in response to CAR19 transfer.

2024-01-22 | GSE193696 | GEO

Signaling in microglia during CAR Tcell induced Immune cell associated neurotoxicity syndrome (ICANS)

Project description:In this experiment, we studied the effect of ICANS on microglial kinase signaling

2024-01-23 | GSE225811 | GEO

Monocyte-derived IL-1 and IL-6 are differentially required for cytokine release syndrome and neurotoxicity by CAR-T cells.

Project description:Single-cell transcriptome profiling using a 3' droplet-based platform (Chromium,10x Genomics) of human CD45+ leukocytes isolated from leukemic HuSGM3 mice infused with CD19.28z CAR-T cells, two days after cytokine release syndrome (CRS) onset and 5 days later.

2018-05-24 | E-MTAB-6505 | biostudies-arrayexpress

Microglia activation during CAR T cell induced neurotoxicity is dependent on TGF-β-activated kinase-1

Project description:Microglia activation during CAR T cell induced neurotoxicity is dependent on TGF-β-activated kinase-1

| PRJNA797269 | ENA

Monocyte-derived IL-1 and IL-6 are differentially required for cytokine release syndrome and neurotoxicity by CAR-T cells.

Project description:Monocyte-derived IL-1 and IL-6 are differentially required for cytokine release syndrome and neurotoxicity by CAR-T cells.

| PRJEB29431 | ENA

Defining the microglia transcriptome in multifunctional protein-2 deficient mice

Project description:Purpose: We purified whole brain microglia of MFP2 knockout mice and control mice utilizing percoll gradient and FACS sorting, followed by microarray analysis to define the molecular changes in MFP2 knockout mice at the endstage of the disease. We compared the microglia transcriptome of Mfp2-/- microglia to that of SOD1-G93A microglia isolated from spinal cord to define the microglia signature associated with a non-neurodegenerative environment. Results and conclusions: Mfp2-/- microglia acquire an activation state characterized by activation of mammalian target of rapamycin (mTOR). In addition, activated microglia display reduced expression of genes that are normally highly expressed by surveillant microglia in steady-state conditions. The immunological profile of is heterogeneous and encompasses upregulation of both pro- and anti-inflammatory genes. In contrast to the neurodegeneration-specific microglia profile in SOD1-G93A mice, Mfp2-/- microglia do not induce genes associated with phagocytosis, lysosomal activation and neurotoxicity. 4 MFP2 knockout and 4 control samples were subjected to microarray analysis.

2015-04-14 | E-GEOD-66420 | biostudies-arrayexpress

Project description:Chimeric antigen receptor (CAR) therapy targeting CD19 is an effective treatment for refractory B cell malignancies, especially acute lymphoblastic leukemia (ALL). While a majority of patients will achieve a complete response following a single infusion of CD19 CAR T cells, the broad applicability of this treatment is hampered by severe cytokine release syndrome (CRS), which is characterised by fever, hypotension and respiratory insufficiency associated with elevated serum cytokines including interleukin-6 (IL-6). CRS usually occurs within days of T cell infusion at the peak of CAR T cell expansion. In ALL, it is most frequent and more severe in patients with high tumour burden CRS is often responsive to IL-6 receptor blockade, but may require intensive life support and further treatment with high dose corticosteroids to prevent potentially lethal severity. Improved therapeutic and preventive treatments require a better understanding of CRS physiopathology, which has so far remained elusive. We report here a murine model of CRS that develops within 2-3 days of CAR T cell infusion, may be lethal and is responsive to IL-6 receptor blockade. We show that its severity is mediated not by CAR T cell-derived cytokines but by IL-6, interleukin-1 (IL-1) and Nitric Oxide (NO) produced by recipient macrophages. This CRS mechanism enables novel therapeutic interventions.

2018-05-28 | GSE111236 | GEO

Chromatin state of mTEClo/int in the RipmOVAxOTII mTEC/Tcell crosstalk mouse model

Project description:mTEC/Tcell crosstalk drives epigenetic programs conditioning immunological tolerance

2022-01-24 | GSE144680 | GEO

mTEClo/int RNAseq profiling in three mouse models of impaired mTEC/Tcell crosstalk

Project description:mTEC/Tcell crosstalk drives transcriptional and epigenetic programs conditioning immunological tolerance

2022-01-24 | GSE144650 | GEO

Project description:CAR T cell related cytokine release syndrome mouse model

| PRJNA436240 | ENA